I will try to find out the clinical scenario regarding his presentation and will add it here if I can find it.
UPDATE 15/04/2013
Pt has a history of congestive cardiac failure, hypertension, hypercholesterolaemia and previous atrial flutter.
Presented with palpitations with no chest pain or SOB when this ECG was taken.
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INTERPRETATION:
ReplyDelete(1.) Atrial tachycardia (rate about 208/min) with . . .
(2.) . . . 2:1 A-V conduction reducing the ventricular rate to about 104/min.
(2.) left bundle-branch block (LBBB).
(3.) Left axis deviation (LAD).
Rate 108
ReplyDeleteRhythm regular
Axis- left axis deviation
P waves normal and normal PR
QRS- prolonged 160ms
Q waves II, III, aVF
LBBB
ST elevation 3mm in V2, 4mm in V3, 2mm in V4
Appearance convex
Interpretation.
Patient is pain free.
Leads V2 and V3 are suggestive of Wellan’s Syndrome. A pattern that can occur after the resolution of chest pain in patients that have proximal LAD lesions.
This pattern requires early cardiac catherisation
Rate approx 100BPM
ReplyDeleteRhythm - regular sinus
Axis - LAD
Normal P waves and normal PRI
QRS widened approx 160ms
LVH - RavL + Sv3 approx 38mm
LBBB - appropriate ST discordance to QRS complexes
U waves seen in lead II - fusing with T waves in most of the precordial leads.
QU in R precordial leads approx 400ms - corrected approx 510ms.
QT in lead II approx 280ms - corrected approx 360ms.
Interpretation:
Sinus tachycardia
LBBB / LAD / LVH
U waves with prolonged QU interval
Consistent with hypokalemia - consider diuretic use
Welcome Brian to the blog comments.
ReplyDeleteThe full interpretation of the ECG will be up tomorrow but this ECG is a bit tricky and I just wanted to go over somethings people have commented on.
Regarding the U waves I agree there is suggestion of one in lead II, in the precordial leads I think you are just seeing prominent T waves with notching due to superimposed atrial activity. I agree there is QT prolongation especially in the precordial leads but I'm not sure of the cause, ?arrhythmia related, ? meds, ? electrolyte.
Clare mentioned the ST segement changes in leads V1-4 which in this case are secondary to underlying LBBB. The Sgarbossa or modified Sgarbossa criteria can be used when considering acute STEMI in the setting of LBBB or paced rhythm. You can read more about the Sgarbossa criteria here and the modified criteria here.
Regarding Wellen's syndrome you are correct that it signifies a potential critical LAD lesion, the ECG features are described as either inverted T waves or biphasic T waves in leads V2-4. There are some great examples of Wellen's on Life in the Fast Lane here.
This ECG's precordial changes are due to LBBB and the notching in the T wave is from p wave superimposition.
Thanks,
John L
DDX atrial tachycardia with block --???digoxin
ReplyDeleteatrial flutter with 3:1 block
Not convinced about presence of flutter waves and if all the waves are p waves, they seem of varying morphology ?MFAT
I know there are only 2 p waves but wonder whether another is getting lost in T waves in limb leads - grossly different p wave morphologies in II - hence my decision to call it a u wave and link to prolonged QU. CCF and HTN - likely to be on diuretic therapy - hence speculation re hypokalemia. CCF and previous flutter - could be on digoxin - AT with block.
ReplyDelete